Erik S. Knudsen, Charlene R. Sexton and Christopher N. Mayhew Pages 749 - 757 ( 9 )
The retinoblastoma tumor suppressor (RB) is functionally inactivated at high frequency in human cancers. Based on the role of RB as a negative regulator of cell cycle this event would be expected to contribute to deregulated proliferation. However, evidence suggests that loss of RB not only mediates aberrant proliferation, but compromises the fidelity of cell cycle transitions leading to a breakdown in genome integrity. This review is focused on the mechanisms underlying this facet of RB function and the contibution of this process to tumorigenesis.
Cell Cycle, E2F pathway, RB interaction, Centrosome Duplication Cycle, DNA replication
Department of Cell Biology, University of Cincinnati, Vontz Center for Molecular Studies, 3125 Eden Avenue, Cincinnati, OH 45267-0521, USA.